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badalkumar,bo-503, b.optm

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badalkumar,bo-503, b.optm

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ankitsingh25320
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TOPIC NAME: AMBLYOPIA

NAME: BADAL
DEPARTMENT: B.OPTM
ROLL NO.: 21001722001
REG.NO.: 222101210001
PAPER NAME: CLINICAL REFRACTION-2
PAPER CODE: BO-503
DEFINITION:
Amblyopia is the unilateral, or rarely bilateral, decrease in best-
corrected visual acuity
• caused by form vision deprivation and/or abnormal binocular
interaction, for which there is
• no identifiable pathology of the eye or visual pathway.
CLASSIFICATION:
1. Strabismic amblyopia
2. Stimulus deprivation
3. Anisometropic amblyopia
4. Bilateral ametropic amblyopia
5. Meridional amblyopia
Strabismic amblyopia:
• Amblyopia seen in those patients with unilateral constant
squint who strongly favour one eye for fixation.
• Typical Features
Grating acuity is better than snellen's acuity
 Always unilateral
 More often in esotropes than exotropes
 Very rare in hypertropia (anomalous head posture)
 Do not occur in alternate strabismus.
Stimulus deprivation
Amblyopia of Disuse
Amblyopia ex anopsia
Amblyopia resulting from those conditions wherein one eye is totally
excluded from seeing early in life.

Monocular congenital or traumatic cataract, complete ptosis, corneal


opacity, prolonged patching of the normal eye for the treatment of
amblyopia etc.
Features:

Most damaging and difficult to treat

Amblyopic visual loss resulting from U/L deprivation is worser


than that produced by B/L deprivation of similar degree. This is
because, in U/L deprivation, interocular effects add to image
degradation
Anisometropic amblyopiaL:
Amblyopia caused by a difference in refractive eior between the
eyes and may result from a difference of as little as 1.0 D sphere
• More common in anisosohypermetropia than in those with
anisomyopia,
• Strabismus is frequently associated with anisometropia and
hence both strabismic amblyopia and anisometropic amblyopia
can coexist.
Meridional amblyopia :
• In patients with uncorrected astigmatic refractive error due to
selective visual deprivation at certain special orientaion,
• Even small amount of U/L astigmatism may cause amblyopia

Bilateral ametropic amblyopia:


Amblyopia results high symmetrical refractive errors, usually
hypermetropia (+5.0D).
 Myopia in excess of -10.0 D also can induce B/L amblyopia
• Astigmatism > 2.5 D
PATHOGENESIS & PATHOPHYSIOLOGY:
Still not elucidated fully
⁃ Amblyogenic Factors
 Role of retina
⁃ Active cortical inhibitio
Amblyogenic Factors:
Form vision deprivation all forms
• Light deprivation –strabismic
• Abnormal binocular interaction - all monoocular forms

Neuropnysiologic stuaies :
-Hubel and Wiesel
Deprivation Studies
By suturing the eyelids of experimental animals
• Observations:
In the LGB, cells in those layers receiving input from deprived
eye showed a profound shrinkage,. Cells of primary visual cortex
either lost their ability to respond to stimultion or showed
significant functional deficiency.
 Conclusions:
 Visual deprivation produces amblyopia by changes in the
visual system neurons.

 Deprivation during the early part of the critical period of


development is more deleterious

Amblyopia produced by binocular deprivation was less


severe than that produced by uniocular deprivation.
Role of Retina:
There is some evidence that the retina itself is abnormal in
amblyopia.
• Decreased sensitivity of foveal cones in amblyopia
• Quicker dark adaptation
• However V.A is reduced disproportionately to reduction in
cone function,
• ERG - Normal
Active Cortical Inhibition:
•Physiologic Evidence - Perhaps the normal eye may ve
responsible for an active cortical inhibition in unilateral
amblyopia.s

• Pharmacologic Evidence - Perhaps in amblyopia active


cortical inhibition might be mediated by inhibitory
neurotansmitter GABA.

Clinical Charecterisics:
1. Visual Acuity - Difference in 2 lines on V.A chart should
be there to diagonse amblyopia
‣ Recognition Acuity - (Snellen) is more affected than
resolution acuity ( Teller's or VER)and detection acuity
( Catford Drum test)
‣ Grating Acuity is less affected in strabismic amblyopia
 Effec of neutral density filter - when placed i of affected eye
V.A improves by one or two lines

 Crowding Phenomenon - (Separation difficulty) Refers to the


inability of an amblyopic eye to distinguish letters crowded
together. Therefore V.A is better when tested with optotype
charts.
2. Fixation Pattern:
 Central fixation - foveolar fixation
 Eccentric viewing - Extrafoveal point because of central
suppression scotoma.
Fovea still not lost its principal visual direction.
Patient look past the object they have been asked to fix.
 Eccentric fixation - Fovea lost its principal visual direction
 If an image is pojected onto the fovea patient report that the
object is seen in some other direction than straight ahead.

 The Heimann-Bielschowsky phenomenon -


Unusual ocular motility pattern which m: develop years
following uniocular visual loss. Strictly monocular coarse,
pendular vertical oscillations occurring only in the
amblyopic eye.
 Paradoxical eccentric Fixation –
Ordinarily, there develop nasal eccentricity in esotropia and
temporal eccentricity in exotropia, Reverse is called paradoxical
fixation.
- surgical overcorrection of deviation
- spontaneous reversal of deviatio

• Absolute central scotoma:


Localisation of object of regard - normal in patients with
amblyopia & eccentric fixation but abnormal in eccentric viewing.

• Colour Vision -Impaired only if V.A is below 6/36. Related to


eccentric fixation.
• Light Perception & Form vision - Dissociated.
• Pupillary light reflexes - generally normal. RAPD may occur in
deep amblyopia.
 Light and Dark Adaptations - Usua normal. Difference in
the region of Kohlrausc. bend (bend in the adaptation curve) has
been found.
• Critical Flicker Frequency - Central CFF tends to approach
that of periphery or of rod mechanism. Also, CFF is faster in
eccentric fixation.
• ERG & EOG -ERG is normal but EOG shows unsteadiness of
fixation.

EVALUATION AND DIAGNOSIS:


• Evaluation of V.A & Refraction
• Neutral density filter test
• Test for crowding phenomenon
• A/S and fundus examination
• Evaluation of fixation
• Other sensory anomalies
Prism Induced Tropia Test :
• 25-D Base in Prism Test : It induces large esotropia creating
diplopia. So normaly infant will not attempt to see through he
prism but if it shows prefernce still, indicates amblyopia in the
uncovered eye.
• Vertical Prism Test : 10-15 D vertical prism is used to induce
diplopia
• CSM method of Rating : C- Central, S- Steady, M- Maintained
(orthotropic)
Evaluation of Central Vs Eccentic Fixation :
1. Angle kappa method –
• Hand light method - Occlude the non fixing eye, ask the
patient to fix at light held directly below patient's eye. Same
repeated on the other eye. Corneal reflex is noted. Angle is
positive, if reflex is displaced nasally and negative,if
displaced temporally. In eccentric fixation, significant
difference in location of corneal reflex will be noted.
• Arc Perimeter Method –
Patient is asked to fi at the central mark on the perimeter. A very
fin is moved along the arc until the light refel is centered on the
cornea. Location of light on the perimeter arc tells the angle kappa
in degrees.
• Major amblyoscope Method - Using special slides with
synoptophore
2. Visuscope Method - In patients above 4-5 years
3. Haidinger's brushes Method - Patient is made to percieve the
entopic pattern of Haidinger brushes and asked to touch is center.

4. Maxwell's spot Method –


Round dark purplish snot X of about 3 arc degrees in d.m. It is
percieved entopically when the eyes are exposed to homogenous
blue or purple field. In eccentric fixation Maxwells spot is
displaced to the side of fixation target.
Management of Amblyopia:
 Prevention and Early Detection
 Treatment of Amblyopia
TREATMENT:
Elimination of cause of Visual depriation -eg congenital
cataract, congenital ptosis,corneal opacity

 Correction of refractive error and spectacle adaptation


should be fully tried before starting occlusion therapy.

Correction of ocular dominance : Occlusion therapy,


penalization, active stimulation,pleoptics, pharmacological
manipulation.
Occlusion therapy:
• Methods - Patch on skin, gauze pad and tape, use of Doyne's
rubber occluder, opaque contact lens etc.
• Timing- Amblyopia Treatment Studies (ATS)
➤In children (3-7y) with severe amblyopia full time patching
produced a similar effect to that of patching for 6 hours a day
➤In children (3-7y) with moderate amblyopia 2 hours of daily
patching produced same improvement as to that of 6 hours.

➤In children (7-13y) prescribing 2-6 hours of patching can improve


visual acuity even if amblyopiahas been previously treated
➤In patients (13-18y) precribing 2-6 hours of patching might
improve visual acuity, but not if amblopia Rx has already been tried
previously.

Active vision exercises by amblyopic eye during occlusion; simple


tasks such as joining dots to make drawing, tracing, threading beads,
watching t,v, reading comics, may enhance visual improvement.
• In patients with visual improvement
assessedmonthly follow up visits, occlusion should be
continued till equal vision and equal fixation
preference is achieved
• Younger the patient, better is the visual
improvement.
• In patients wits no improvement on 3 monthly follow
up, futher occlusion is unlikely to be fruitful
• Management Occlusion Treatment - Once the vision
has ben equalised occclusion therapy for 2-3 hours
has to be continued till atleast 9yrs.
.
Pharmacological Manipulation:
• Levodopa, a precursor for catecholamine dopamine has been
studied as an adjunct ti patchinf, but remains controversial.

Role of perceptual learning:


• It employs practicing a visual discrimination task eg;
Positional acuity, Contrast acuity, Stereo acuity etc.
• Recommended period for perceptual learning is2hrs/day, 5
days/ week, for a period of 9 months.
• Still controversial
ACKNOWLEDGEMENT
I would like to thank my teacher or in the
TANUKA CHAKRABORTY who gave the
opportunities to work on this preparation I go to
learn a lot this presentation about exploring career
opportunity I would have also like to thank your
principal Dr Sudpa Chakraborty at last would like
to extend my heart full thanks to my parents
because without their help this presentation of not
have been successful finally I would like to thanks
to my friends who have been with me all the time
BADAL KUMAR
B.OPTM

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